Unveiling the Atropine Effect on Heart Rate

Atropine is commonly used in clinical medicine. This product is an anticholinergic drug, which can block acetylcholine and myocardial M2 receptor binding. Also, it can reduce the vagus nerve effect and accelerate heartbeat. However, atropine's effects are not always positive and sometimes cause a slow heartbeat. Therefore, this article intends to explore the atropine effect on heart rate for clinical use.

What is atropine?

Datura was probably the world's first painkiller. Theophilus, an ancient Greek scientist, discovered in the fourth century B. C., that datura can be used to treat pain, gout, and insomnia. In the first century, it was found that soaking a datura in wine could cause paralysis, which could be used to treat pain and insomnia, before surgery, or when burning. In 1831, German pharmacist Mein successfully obtained the pure crystallization of atropine from datura stramonium, and the first formal human encounter with atropine. 

Atropine is found naturally in many plants of the genus Solanum, including the deadly plants belladonna, datura, and mandrake. Atropine is a drug used to treat certain types of neurotoxic and pesticide poisoning, as well as certain types of bradycardia, and to reduce saliva production during surgery.

Atropine is used either intramuscularly or intravenously. Eye drops can be used to treat uveitis and early amblyopia. Intravenous administration generally can be effective in a minute, acting for half an hour to an hour. Large doses are necessary for some poisoning. The atropine effect on heart rate is a double-edged sword.

How Is Atropine Used to Treat Bradycardia? 

Atropine reversible antagonizes the cholinergic M receptor and inhibits parasympathetic excitation. Parasympathetic nerves are widely distributed in the sinoatrial node and the atrioventricular node, so atropine can block the parasympathetic nerves and improve the function of the sinoatrial node and the atrioventricular node. 

The heart has parasympathetic and parasympathetic nerve structures, of which the parasympathetic nerve accounts for the absolute majority of the heart rate and has a great impact. In 2018, the ACC/AHA guidelines for bradycardia block in the United States listed atropine as an IIIa class drug to improve sinus node function and atrioventricular nodules, better than beta-agonists. The conduction system of the Hispanic bundle and below is less regulated by parasympathetic nerves, so atropine has little effect on the block of the Hispanic bundle and below.

In addition to the heart, the parasympathetic nerve is also responsible for the functional regulation of many other organs. After taking atropine, patients will appear dry mouth, no sweat, blurred vision, intestinal peristalsis, urine retention, and other adverse reactions.

Atropine is a safe and effective method to treat myocardial ischemia, but we should avoid the increase in heart rate, otherwise, it may aggravate the risk of myocardial ischemia. In rare heart transplant patients, atropine does not increase heart rate because their parasympathetic nerves have been lost.

The effect of atropine on sinus node function varies with dosage. A low dosage (< 0.5 mg) can accelerate heart rate, and a large dosage can accelerate heart rate. Therefore, atropine should not be given at the beginning of 0.5~1mg. The speed of static push should be faster. If necessary, it should be repeated every 3~5 minutes and the maximum dose should be 3mg.

Atropine half-life is only about 2 hours for adult patients and can only slow the heart rate in the short term. Muscular and subcutaneous administration, unlike intravenous administration, is slow, and low concentrations in the blood can slow the heartbeat, which is an incorrect form of medication.

Why does a low dose of atropine cause bradycardia?

Receptors that bind specifically to acetylcholine (ACh) are known as cholinergic receptors and can be categorized as M and nicotine (N) receptors. According to pharmacological classification, M receptors can be divided into five subtypes: M1, M2, M4, M5, M1, M2, and M3.

When ACh binds to an M-type receptor, it produces a series of parasympathetic excitatory effects, including inhibition of heart activity, contraction of bronchial smooth muscle causing airway spasm, contraction of gastrointestinal smooth muscle causing gastrointestinal colic, contraction of bladder detrusor promoting urination, and stimulation of digestive and sweat gland.

Atropine is the most commonly used M receptor antagonist in the clinic, which has a dose-dependent excitatory or inhibitory effect on the central nervous system. Tropine has a strong effect on cardiac M2 receptors.

At low doses, blocking the M1 receptor on the presynaptic membrane of the parasympathetic ganglionic fibers and stimulating the release of acetylcholine (ACh) may lead to a short and mild slowdown in some patients, which is not associated with changes in blood pressure and cardiac output.

In normal patients, a 0.4-0.6mg dose of atropine may cause a transient mild heart rate to slow down as tissue drug levels increase. This generally lasts a short time and has little impact.

However, drug distribution in patients with cardiogenic shock is usually delayed. Thus, in peri-shock patients with bradycardia, the duration of this bradycardia exacerbation may be prolonged and may cause clinical harm.

Conclusion

The atropine effect on heart rate is related to its dose. In small doses, this medicine can slow the heart. Higher doses of atropine can cause your heart to beat faster, and can even be fatal if overused.